Arterial supply to brain:Circle of Willis configuration and common variations
Circle of Willis is formed by an arterial polygon as the internal carotid and vertebral systems anastomose around the optic chiasm and infundibulum of the pituitary stalk. This communicating pathway allows equalization of blood-flow between the two sides of the brain, and permits anastomotic circulation, should a part of the circulation be occluded. Vessels comprising the circle of Willis: # left and right internal carotid arteries (ICA) # horizontal (A1) segments of the left and right anterior cerebral arteries (ACA) # anterior communicating artery (ACOM) # left and right posterior communicating arteries (PCOM) # horizontal (P1) segments of left and right posterior cerebral arteries (PCA) # basilar artery (tip) The anterior circulation is comprised of vessels 1-3 and their branches; the posterior circulation arises from vessels 4-6 and their branches. Together these supply the cerebral hemispheres and the mid brain. The perforating branches of the arteries are terminal supplies with no pre-capillary anastomoses. Formation: * The basilar artery divides at the upper border of the pons to form the left and right PCAs. * From each ICA, a PCOM arises at the anterior perforated substance and runs back through the interpeduncular cistern to join the ipsilateral PCA. * Each ICA also gives off an ACA. The ACAs are united by the ACOM, a small vessel that runs in the chiasmatic cistern (below the rostrum of the corpus callosum), to complete the circle. Other branches: Supply optic chiasm and tracts, infundibulum,hypothalamus and other structures at base of brain: * medial lenticulostriate arteries (from A1 segment of ACA) * thalamoperforating and thalamogeniculate arteries (from basilar tip, proximal PCAs and PCOMs) * perforating branches (from the ACOM) Vascular Territory * Vascular distribution of ACA, MCA, PCA vary from individual to individual, have typical as well as maximum, minimum territories * Two vascular "watershed" zones exist at confluence of territorial supply, are vulnerable to hypoperfusion ** Cortical watershed = subpial confluence of cortical ACA/MCA/PCA branches ** Deep white matter watershed zone = confluence of deep cortical penetrating branches, perforating branches from circle of Willis (COW) * ACA ** Perforating branches: Corpus callosum rostrum, heads of caudate nuclei, anterior commissure, anteromedial putamen/globus pallidus/anterior limb internal capsule (if RAH present) ** Cortical branches: Inferomedial frontal lobes, anterior 2/3 of medial hemisphere surface, 1-2 cm over brain convexity * MCA ** Perforating branches: Most of putamen, globus pallidus, superior half of internal capsule, most of caudate nucleus, some deep white matter ** Cortical branches: Most of lateral surface of cerebral hemispheres, anterior tip (pole) of temporal lobe * PCA ** Perforating branches: Much of central brain base (thalamus, hypothalamus), midbrain, choroid plexus ** Cortical branches: Most of inferior surface of temporal lobe, occipital pole, variable amount of posterolateral surface of hemisphere * BA ** All of PCA territory (including perforating branches), most of pons, superior cerebellum/vermis * VA ** Most of medulla, cerebellar tonsils, inferior vermis/cerebellar hemispheres Variant anatomy A complete circle of Willis (in which no component is absent or hypoplastic) is only seen in 20-25% of individuals. Posterior circle anomalies are seen in nearly 50% of anatomical specimens. Common variants * PCOM ** hypoplasia of one or both ~30% ** infundibular dilatation of the PCOM origin ~ 10% ** duplication * ACOM ** absent or fenestrated ACOM ~12.5% * ACA ** absent/hypoplastic/fenestration A1 segment of ACA ~15% * PCA ** absent/hypoplastic P1 segment (foetal origin of PCA off the ICA instead of the basilar) ~20% * MCA ** duplication or fenestration ~ 3% * Basilar artery fenestration * Vertebral artery fenestration Congenital absence of one or both ICAs may occur but is rare. If one ICA is absent, intrasellar intercarotid communicating arteries are common and there is a high incidence of associated aneurysms. Clinical significance: Aneurysm bleed account for 90% of all SAH. These are found mostly in junctional sites, where vessels branch, e.g. anterior cerebral with anterior communicating, internal carotid with posterior communicating or middle cerebral due to weak tunica media.